Propranolol blocks the tachycardia induced by galanin (1-15) but not by galanin (1-29).

Abstract

The efferent pathways involved in the tachycardia induced by intracisternal injections of the N-terminal galanin fragment (1-15) (GAL (1-15)) and galanin (GAL (1-29)) has been evaluated in rats pretreated with the cholinergic antagonist atropine or the beta-antagonist propranolol. The pretreatment with propranolol significantly blocked the tachycardic and vasopressor effect produced by intracisternal injection of GAL (1-15) (p<0.05), but the pretreatment with atropine did not modify these cardiovascular effects. However, the cardiovascular response elicited by GAL (1-29) is modified by the pretreatment with atropine (p<0.05) but not by propranolol. These findings demonstrate that the central cardiovascular action of GAL (1-15), but not GAL (1-29), is mediated by beta-receptor stimulation and this suggests the existence of a different pathway involved in the cardiovascular response produced by the N-terminal galanin fragment as compared with the parent molecule GAL (1-29).

• Authors: Zaida Díaz-Cabiale, M Paz Cordón, Rafael Coveñas, Alicia Rivera, Noboru Yanaihara, Kjell Fuxe, Salvador González-Barón, José A Narváez
• Journal: Regulatory peptides (Regul Pept) Vol. 107 Issue 1-3 Pg. 29-36 (Jul 15 2002) ISSN: 0167-0115 [Print] Netherlands
• PMID: 12137963 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Peptide Fragments
• galanin (1-15)
• Atropine
• Galanin
• Propranolol

Topics

• Animals
• Atropine (pharmacology, toxicity)
• Blood Pressure (drug effects)
• Cisterna Magna
• Galanin (antagonists & inhibitors, toxicity)
• Heart Rate (drug effects)
• Male
• Peptide Fragments (antagonists & inhibitors)
• Propranolol (pharmacology)
• Rats
• Rats, Sprague-Dawley
• Tachycardia (chemically induced, drug therapy)
• Time Factors